![]() |
||||
![]() |
||||
|
|
Jiandong
Chen, Ph.D. E-mail:Jiandong.Chen@moffitt.org Training Research Interests Over 50% of human tumors have mutations in the p53 tumor suppressor gene. P53 is a transcription factor that can be activated by a variety of stress signals, which then induces a group of genes to inhibit cell proliferation or induce cell death. We are interested in studying how p53 is normally regulated and how it is inactivated in tumors without undergoing mutations. An important regulator of p53 is the MDM2 oncogene, which can inactivate p53 by promoting its degradation. We are trying to identify drugs that can block MDM2 function and activate p53 in tumor cells. Such drugs may be useful for cancer treatment. Our laboratory is also studying other p53-like proteins that are present in human cells by creating temperature-sensitive mutants of the p53 homologs p63 and p73. These proteins can also block tumor growth when produced at high levels. Therefore, understanding how they are regulated and identifying ways to induce these p53 homologs may provide a novel means to inhibit tumor growth. Selected
Publications 2. Lihong Chen, Wenge Lu, Sudhir Agrawal, Wenqiang Zhou, Ruiwen Zhang, and Jiandong Chen. (1999). Ubiquitous induction of wild type p53 in tumor cells by antisense inhibition of mdm2 expression. Molecular Medicine. 5:19-32. 3. Radhika Pochampally, Brent Fodera, Lihong Chen, Wenge Lu, and Jiandong Chen. (1999). Activation of an MDM2-specific caspase by p53 in the absence of apoptosis. J. Bio. Chem. 274:15271-15277. 4. Xiaoya Zeng, Lihong Chen, Christine A. Jost , Roth Maya, William G. Kaelin Jr., Moshe Oren, Jiandong Chen and Hua Lu. (1999). MDM2 Suppresses p73 Function by Inhibiting p73-p300/CBP Interaction without Promoting p73 Degradation. Mol. Cell. Biol. 19:3257-66. 5. Wenge Lu, Radhika Pochampally, Lihong Chen, Mullika Traidej, Yiliang Wang, and Jiandong Chen. (2000). Nuclear exclusion of p53 in a subset of tumors requires MDM2 function. Oncogene. 19:232-240.
|
|||
|
|
||||